The primary aim of this work is to ascertain the role of prostaglandins, the renin-angiotensin system and certain neurogenic mechanisms in the regulation of blood flow in certain vascular beds. We will determine the relative capacity of the normally perfused and pump perfused paw vascular bed to synthesize prostaglandins from arachidonic acid. Prostaglandins in the paw venous blood will be measured by radioimmunoassay. The influence of repetitive i.a. doses of norepinephrine on the synthesis of PGE will be determined. Clonidine give intravertebrally has been found to augment chemoreceptor induced vasoconstrictor responses in the skeletal muscle bed. We plan to ascertain whether this effect of clonidine can be blocked centrally by alpha receptor blockers. We will also attempt to potentiate the chemoreceptor induced response in the cat by electrical stimulation of the nucleus solitarius. We will compare the relative direct and adrenergic potentiating effects of angiotensin II and the des asp-angiotensin II analogue on the isolated tibial artery and the pump-perfused paw. We will determine whether prostaglandin E suppresses the facilitation of nor-epinephrine release brought above by angiotensin II in the renal vascular bed. Catecholamines in the renal venous blood will be measured during renal nerve stimulation before, in the presence of angiotensin, and in the presence of angiotensin after prostaglandin synthesis inhibition by meclofenamate. BIBLIOGRAPHIC REFERENCES: Influence of the renin-angiotensin system on the effect of prostaglandin synthesis inhibitors in the renal vasculature. Satoh, S. and B. G. Zimmerman. Circ. Res. Suppl. to Vol. 36 & 37, Suppl. I, 1975. Effect of angiotensin antagonist, 1-sarcosine-8-alanine angiotensin II on renal vascular resistance. Satoh, S. and B. G. Zimmerman. Am. J. Physiol. (in press).